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AC Fat Loss Bible critique part II

On to the second and, mercifully, final part of the critical review of the metabolic advantage as presented by A Colpo in his book The Fat-Loss Bible. As discussed in the previous post, our friend, like the kid to the left, is focused so intently on his refusal to believe in even the possibility of the existence of a metabolic advantage that he can’t read the literature correctly – not even the very literature he uses to try to prove his own position. His bias has hypnotized him to the point that he can’t see anything that doesn’t confirm his what he already believes. And this same bias prevents him from even taking a scientific approach to the problem.

We all fall victim to the confirmation bias and have to fight it constantly. Gary Taubes thinks I may even have succumbed a little in the earlier post on AC and the metabolic advantage. He emailed me saying he had read the post and thought it was great up to the point right at the end where I wrote that the data on the whole showed that, if anything, there was a metabolic advantage. Gary thought the data presented in all the studies in AC’s chart was ambiguous and that I was going out on a limb a little in making the statement that I thought, if anything, that the papers argued for a metabolic advantage.

I disagree.

I decided to base this critique not on the scientific literature at large, but instead on only the papers that AC mustered for his argument. I intended to make the critique much like a court case in which one side presents the information and the other attempts to counter it. I didn’t want to go out myself and gather a bunch of papers that confirmed my viewpoint, because then we would have had nothing but a bunch of dueling Ph.Ds, a bunch of he saids, she saids, that wouldn’t prove anything. I stuck with the papers AC used and presented my arguments as to why I didn’t think his papers proved his case. After going back and rereading the post, I still feel that if this ‘evidence’ were presented to a jury, the verdict would come back in favor of my arguments. If anything, AC’s own ‘evidence’ argues for the existence of a metabolic advantage, and, at worst, certainly doesn’t ‘prove’ that one doesn’t exist.

Since I posted the first part of my critique, AC has responded using his customary restraint and understated gentility designed to appeal to his sort of reader. His response – as I figured it would be – is merely a listing of even more papers he believes substantiate his claims. Instead of undertaking a serious scientific inquiry, he is looking for more white swans. Let me explain.

I wrote a long post a couple of years ago on Sir Karl Popper and the metabolic advantage. Popper set the standards by which hypotheses should be structured. A well-stated hypothesis should be able to be falsified. That doesn’t mean it will be falsified, but it should be structured in a way that it can be. And real scientists – of which, sadly, there are all too few in the field of nutrition – don’t try to confirm their hypotheses: they try to refute them.

One of the examples Popper used in explaining how a hypothesis should be established involved swans – white and black. He used the following as an example of a good hypothesis: All swans are white. He made the case that this hypothesis cannot be confirmed by simply pointing out more and more white swans. The hypothesis can be strengthened by doing so, but it can’t be proven. It can, however, be disproved by the discovery of even a single black swan. Popper argued that scientists should be working to find black swans instead of simply adding more and more white swan sightings to their data. The more effort scientists expend to find a black swan without finding one, the more their hypothesis is strengthened. Diligently searching for black swans is a much more valid scientific endeavor than simply looking for more white swans.

Many scientists don’t want to hunt for black swans, however, because they don’t want to blow up their hypotheses. The easy way to bolster their hypotheses is to continue to tally up all the white swans they find and forget about looking for black ones.

Which, of course, is what our young friend AC has done and written about in his latest missive. He tallies up a bunch more white swans and ignores the black ones, even the black ones in hiding in plain sight in his own list of papers. This failure of his to try to puncture his own hypothesis leads me to believe there exists a large chasm of incomprehensibility between the way AC thinks and the scientific method.

To give but one example of this, AC argues in his book that the studies by Rabast that clearly show a metabolic advantage aren’t valid because, as AC puts it,

Regardless of whether Rabast et al’s findings were the result of water loss from glycogen depletion, pure chance, or some other unidentified factor, they should be regarded for what they are: An anomaly that has never been replicated by any other group of researchers. For a research finding to be considered valid, it must be consistently reproducible when tested by other researchers. As proof of the alleged weight loss advantage of low-carbohydrate diets, the findings by Rabast and colleagues fail dismally on this key requirement.

(In other words, AC is saying: that black swan over there isn’t really a black swan, because all the other swans I’ve pointed out are white. And since all the others are I’ve pointed out are white, that one can’t be black. It’s impossible.)

In point of fact, Rabast’s group in Germany has performed a number of studies showing a significant metabolic advantage in subjects in metabolic wards who follow low-carb, high-fat diets as compared to those taking in the same number of calories as high-carb, low-fat diets. This group pursued this line of inquiry and published a number of studies showing this metabolic advantage. Suddenly, however, they quit publishing on this subject and turned their attention elsewhere.

While in the research phase for Good Calories, Bad Calories, Gary Taubes interviewed Dr. Rabast about his group’s work, and here is what he said. They were inspired by an old scientific paper (more about which later) that offered up some data they found interesting and wanted to test themselves. They did the studies using formula diets, so they could more easily control intake and confirmed the data from the old study. They continued to perform these studies, all with similar outcomes, until Dean Ornish published his paper on dietary fat and heart disease. Dr. Rabast and his group decided that Ornish might be correct. They felt that although their own data showed that high-fat diets brought about substantially better weight loss than low-fat diets of equal calories, their work might encourage people to consume more fat, which, thanks to Ornish and the low-fat movement, they had come to believe may cause heart disease. So, they abandoned their research on high-fat diets and moved on to other interests.

The study that inspired them to study high-fat diets? An study from the 1950s done by a couple of British researchers, Dr. Alan Kekwick and Dr. G.L.S. Pawan. Their famous paper showed a definite metabolic advantage, a black swan writ large, as it were. And their famous paper is well known to AC, who has a few things to say about it. As you might suspect, given the results of this study, he declares it not worthy of consideration. Here is what he says in his book after he’s gone through his list of white swan studies, which, of course, are all worthy of mention.

Not-so-worthy mention

There is one metabolic ward trial that due to its short duration did not qualify for inclusion in Table 1a, but still warrants a mention. Incessantly cited by supporters of low-carb diets, this is the famous metabolic ward study conducted in the 1950s by Kekwick and Pawan. The London researchers conducted two experiments. In one of these, they claimed that patients maintained or gained weight on a typical mixed diet of 2,000 calories, yet consistently lost weight when placed on a 2,600 calorie low-carbohydrate diet for periods ranging from 4 to 14 days. In the second of their experiments, they had 14 patients alternate between four different 1,000 calorie diets, spending a grand total of 5-9 days on each diet: 1) 90 % protein; 2) 90% fat; 3) 90% carbohydrate, and; 4) a mixed diet. According to Kekwik and Pawan, all of the subjects in the protein, fat, and mixed diet groups lost weight, with the high-fat group experiencing the greatest weight loss of all. However, despite the very low calorie intake, many of the patients reportedly gained weight during the high-carbohydrate diet! Not surprisingly, the Kekwik and Pawan study is frequently cited by supporters of low-carbohydrate nutrition. That they ignore the studies in Table 1a, yet eagerly embrace a short-term study conducted over 50 years ago, speaks volumes about their complete disregard for rational scientific inquiry. [Italics in the original]

Here’s why: Firstly, it has long been known that in the first week or two of low-carbohydrate dieting, there is often a far greater reduction in water weight due to excretion of sodium and/or glycogen, both of which bind water in the body. Therefore, studies of such short duration are next to useless as indicators of the comparative longer-term weight loss effects of these diets.

Secondly, the Kekwik and Pawan study was a poorly controlled mess. The researchers were even driven to denigrate their study participants, writing: “The first and main hazard was that many of the patients had inadequate personalities. At worst they would cheat and lie, obtaining food from visitors, from trolleys touring the wards, and from neighbouring patients. (Some required almost complete isolation.)” [Italics in the original]

Given that protein and fat have been shown numerous times to exert satiating effects, while low-fat, high-carbohydrate diets (especially the liquid, low-fiber variety!) typically result in ravenous hunger, it’s not hard to guess during which diet the participants may have ‘cheated’ the most!

The researchers also wrote: “The results we report are selected, a considerable number of known failures in discipline being discarded”. Note how the researchers included the words “known failures”; how many failures did they not know about? How many of the patients were crafty enough to sneak extra food without being caught? Why should we trust Kekwik and Pawan’s unlikely results, given their study’s numerous flaws? The answer is simple: Unless you are a famous low- carb diet ‘guru’ who has made millions promising people they will lose extra weight at the same calorie intake by cutting carbs, we shouldn’t! At least not if we believe good science mandates a tightly controlled process of investigation. [Italics in the original]

It is apparent from his critique that AC read the first part of this study, found a black swan, used a bunch of incorrect gibberish and swagger to try to say it wasn’t really a black swan and moved on without ever getting to the important part of the paper. Or, an alternative explanation is that, as with the Leibel study mentioned in my first critique, he either didn’t really read the paper thoroughly or he seriously misunderstood what he read.

Drs. Kekwick and Pawan start off by explaining why they undertook this study in terms that any of us who have struggled with excess weight and found different results with different diets can understand.

Many different types of diet have been successfully used to reduce weight in those considered obese. The principle on which most of them are constructed is to effect a reduction of calorie intake below the theoretical calorie needs of the body. Experience with these patients has suggested, however, that this conception may be too rigid. Many of them state that a very slight departure from the strict diet which can hardly affect calorie intake results in them failing to lose for a time. Though it is realized that evidence from such patients is notoriously inaccurate owing to their approach to this particular condition, it is too constant a belief among them to be entirely discarded.

Drs. K & P did a number of experiments. First they kept hospitalized subjects on diets of similar macronutrient composition but differing calories and found that reducing calories made the subjects lose weight. And, unsurprisingly, the more the calories were cut, the more weight the subjects lost. Next, the good doctors decided to see if changing the macronutrient composition of the diets made a difference. They started the subjects on 1000 calorie per day diets of one of the following three structures: 90 percent of calories as carbohydrate; 90 percent of calories as protein; or 90 percent of calories as fat. The structure of the diets made an enormous difference in how much weight the subjects lose. As Drs. K & P wrote:

So different were the fates of weight-loss on these isocaloric diets that the composition of the diet appeared to outweigh in importance the intake of calories.

In an effort to confirm their findings, Drs. Kekwick and Pawan went on to a third series of experiments as described here:

…patients…were put on to 2000-calorie diets of normal proportions to show that their weight could be maintained while in hospital at this level and then placed on high-fat, high-protein diets providing 2600 calories per day. It was demonstrated that these patients on the whole could maintain or gain weight on 2000-calories but, except in one instance, lost weight consistently on a 2600 daily calorie intake.

It’s easy to see why AC doesn’t like this paper. And we haven’t even gotten to the good stuff yet, which AC doesn’t make mention of in his book. We’ll get to that in a bit, but before we do, let’s take a look at AC’s critique of this much of the study (which is, apparently, all he bothered to read). You can read along from the above quote in his book.

His first complaint is that the study is over 50 years old. I find this a strange complaint, since the first study he lists in his chart of studies ‘proving’ his point was published a mere eight years after this Kekwick and Pawan study. The Kinsell paper was published in 1964, 46 years ago. Is there some magic cutoff date at 50 years that makes scientific papers unreliable?

Second, he claims that on low-carb diets all the weight loss from the first two weeks is water, and since these studies lasted less than two weeks, the difference was all water.

Kekwick and Pawan were a little smarter than Anthony gives them credit for being. They understood well the notion of water loss. (As we will see shortly, they understood it vastly better than our young friend.) They pointed out the following:

During these periods [the different diet studies] the patients were weighed daily and in some of them balance studies were carried out in respect of water, nitrogen, fat, sodium, chloride, and potassium. Total body-water and the basal metabolic rate were estimated weekly or at the end of each period on the diet.

If you look at the full-text version of the study I linked to above, you can see graphically how this all plays out. In these studies the weight loss was definitely not all water.

In an effort to be meticulously accurate, not only did K & P monitor all the above carefully, they even went further. Since these patients were not on formula diets but were on real foods instead, making it more difficult to accurately determine caloric intake, the staff would take representative samples of the foods eaten, blend them into a soup, then analyze samples to make sure the protein, carbohydrate and fat content were as estimated in the food tables. It was hardly a “poorly controlled mess” of a study.

AC next attacks the study because the researchers admitted as to how difficult it is – even in hospitalized studies – to prevent cheating.

In such a study the difficulties are formidable. The first and main hazard was that many of these patients had inadequate personalities. At worst they would cheat and lie, obtaining food from visitors, from trolleys touring the wards, and from neighbouring patients. (Some required almost complete isolation.) At best they cooperated fully but a few found the diet so trying that they could not eat the whole of their meals. When this happened the rejected part was weighed, and the equivalent calories and foodstuffs were added to a meal later in the day. The results we report are selected, a considerable number of known failures in discipline being discarded.

Kekwick and Pawan simply wrote of the difficulties in preventing cheating. They were on the lookout for it, threw out data they knew was compromised, and compensated for episodes of cheating of which they were aware. I believe the fact that they recognized cheating as going on and were keeping an eagle eye out for the cheaters makes their data more accurate, not less.

I also find it strange that AC is more than willing to toss data because of cheating in this study and is more than willing to accept data from other studies in which there was probably just as much – if not more – cheating that the authors neglected to mention either by design or because they didn’t realize it was happening.

One other thing that points to the degree into which K & P watched over this study is one that all female readers who have had trouble losing will be familiar with.

Another factor of importance which could not be eliminated was that many patients were women, in whom the retention and the losses of water associated with the menstrual cycle affected the daily weight and the estimation of total body-water. We were surprised to find how great such factors could be, amounting in one woman to the retention of more than 3 litres of water.

Only a fool or a seeker of white swans only would think the good doctors didn’t monitor this study closely.

Now to the fun part, the part AC probably didn’t read. And the part that really demonstrates the metabolic advantage.

The first part of this paper, the part AC has critiqued, is only a minor part of the paper. The majority of the paper is devoted to the efforts the Drs. K & P made to determine what happened to the excess weight lost in dieters on the higher-fat diet. They checked fat loss in the stool, they checked (as mentioned previously) water loss, they checked about everything they could think of. You can read in the full version how careful they were.

After sifting through all the data and finding no reason that their results should have been invalid, the docs checked yet one more item. They looked at insensible water loss.

Insensible water loss is the loss of water we all experience minute by minute that we not aware of. We know we lose water when we urinate and/or defecate, and we know we lose some water when we visibly sweat, but we are not aware of the large amount of water we are getting rid of through our breath and via sweating that we don’t notice. And this amount of water we lose is fairly large.

Do this experiment. Get an accurate scale and weigh yourself immediately before going to bed. Go ahead and urinate (and do anything else you might need to do) before weighing. Don’t drink or eat anything, hop in the sack and sleep through the night, then get up and weigh before you urinate in the morning. I absolutely guarantee that you’ll weigh less than before you went to bed.

If you breathe on a mirror, you will fog it from the water vapor in your breath. This vapor is water that you lose every single time you take a breath. You breathe approximately 12 times per minute (while resting), which means you breathe 720 times per hour and 17,280 times per day. And that’s if you’re at rest. If you are active, you take a lot more breaths than that. Probably something in the neighborhood of 20,000-23,000 breaths per day, depending upon activity level. Each one of these breaths contains water vapor that you are losing from your body, which is why you drink liquids throughout the day. If you didn’t replace this water, you would become dehydrated.

If you have a fever or if you exercise, you breathe a lot more rapidly and lose a lot more fluid. Thus, one of the things doctors have to be concerned about in very sick patients with high fevers is dehydration.

You also lose insensible water through constant perspiration. When you awaken in the morning, if you’ve slept tightly covered up, you’ll notice you’re a little damp. Not a lot, unless you’ve had a fever, but a little. This is insensible water that you lost.

I remember how amazed I was the first time I ever looked at my own hand under a dissecting microscope. Looking at my hand with my naked eye, it appeared normal and dry. When I stuck it under the scope and looked, I could see little volcanoes of perspiration bubbling up from unseen pores. It’s part of the way we regulate our temperature, and unless we work up a visible sweat, we never notice.

This loss of insensible water is why we lose weight overnight. In eight hours of sleep, we breathe out about 5,760 breaths filled with water vapor and we sweat all night. This water weight usually ends up being between 1 to 2 pounds or even a little more.

If I were to take a bunch of thyroid hormone or take an amphetamine, I can assure you that my metabolic rate would rise and that my insensible water loss would increase. In fact, insensible water loss is a surrogate for metabolic rate. If your metabolic rate rises, your insensible water loss rises. And since insensible water loss can be easily measured, the metabolic rate can be easily estimated without having to do metabolic chamber studies.

Which is exactly what Drs. Kekwick and Pawan did with several subjects on the various diets.

They kept the subjects isolated and under supervision and weighed them on extremely accurate scales throughout the day.

Measurements were made by weighing the patient at intervals of one hour on scales specially constructed for this purpose by Messrs. W. & T. Avery Ltd. which are sensitive to 2 g. over the range of weights concerned. During these hours no food was taken and neither urine nor faeces voided, and errors due to temperature, activity, and air draughts were avoided as far as possible.

(Scales that are sensitive to 2 g are extremely sensitive. Two grams weighs about seven one hundredths of an ounce.)

So, here is what the researchers did. They first fed the subjects the standard diet available to the patients on the ward and discovered what the insensible water losses were throughout the day. You can see how this came out in the graph below, Fig. 11.

When Drs. K & P put a single patient on the different diets – 90 percent fat, 90 percent protein or 90 percent carbohydrate – and measured the insensible water loss throughout the day, the table below, Fig. 12 shows what happened. There was an increase in insensible loss with the high-protein diet as compared to the high-carb diet, and a much greater increase in insensible water loss with the high-fat diet.

The area of the chart that I colored in is the difference between insensible water loss, which represents a change in metabolism, between the high-carb diet and the other two diets. This colored part of the chart represents the metabolic advantage of the high-protein and high-fat diets compared to the high-carb diet of the same number of calories. The peach colored part of the chart represents the metabolic advantage of the high-fat diet as compared to the high-protein diet while the grayish color represents the metabolic advantage, as measured by increased insensible water loss, between the high-protein and high-carb diets.

The researchers wanted to make sure this wasn’t an isolated phenomenon, so they analyzed three other patients and created the graph below, Fig. 13, which mirrors the results in Fig. 12 and demonstrates that this wasn’t an outcome isolated to just one subject.

The rate of insensible loss appears to be much affected by the type of food, provided that the water and sodium intakes are kept constant throughout the period of observation; whether this increased rate of insensible loss is a measure of bodily metabolic activity must remain in question. Even if metabolic activity cannot be measured directly, the difference in weight responses seen with these diets does not seem to be completely due either to an altered state of hydration or to a simple deficiency of calories. We suggest that the rate of katabolism of body-fat may alter in response to changes in the composition of the diet.

And their summary:

As the rate of weight-loss varied so markedly with the composition of the diets on a constant calorie intake, it is suggested that obese patients just alter their metabolism in response to the contents of the diet. The rate of insensible loss of water has been shown to rise with the high-fat and high-protein diets and to fall with high-carbohydrate diets. This supports the suggestion that an alteration in metabolism takes place.

If you haven’t already, I would encourage you to read this entire study and make your own judgment. I’m sure you won’t find it the “poorly controlled mess” that AC does. In fact, I suspect you’ll find just the opposite. Unlike most of the studies published today, this one is not loaded with incomprehensible jargon, is delightfully well written and is extremely accessible to those with little medical or scientific knowledge. You can see for yourself how precise these researchers were and now meticulously they looked for anything that might confound their results. It would be great if more studies were done this carefully today and written this clearly.

This is the end. I am through with AC. I’ll leave it to the readers of this post and the previous one on this subject to make their own decisions as to whether or not a metabolic advantage exists for low-carb, higher-fat diets. I won’t be provoked again into jumping into the mud and wrestling around. So this is my black swan song on the subject.

A good foe is far more loyal, far more predictable, and, to the clever, far more useful than any admirer.

So, to you, Anthony Colpo, I raise my hat. Had you not attacked me out of the blue, I would be less knowledgeable than I am today. I wouldn’t have bothered to dig into all the ‘white swan’ papers you posted trying to figure out why these researchers got the results they got. I, like you, would still be mired in the notion that metabolic ward studies are squeaky clean without any hint of sullied data as a consequence of cheating. Like you, I would still probably be confusing metabolic ward studies with metabolic chamber studies, which are horses of a much different color. Also, I thank you because I had kind of blown off the Kekwick and Pawan papers (there are others besides this one from The Lancet) as being too old to be worth studying. You forced me to take another look, and I was delighted at what I found. And, sad to say, like you, I, too, had read only the first part of the these studies, the parts about the diet comparisons. It wasn’t until your attack that I actually read this paper all the way through and found the gold mine in the latter pages.

So, AC, I sincerely hope the best for you; I thank you for pushing me into this exercise and wish you godspeed on your journey through life.

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Interesting how a high number [maybe even the majority] of comments on the first few pages [as far as I read] defend fat intake and carbohydrate restriction. I’m interested to read the papers he cites as demonstrating worsening CV outcomes on Atkins. The headline says something about LC making people ultimately fatter, but I didn’t see anything in the body to support that.

I don’t yet have the articles in hand that Ornish cited for LC diets worsening CV outcomes, but I did read the findings as described by the authors in the PNAC study he cites, and reported by Science Daily. This was a 12-week study with ApoE mice, in which LC diet was defined as high protein. All the carbohydrate calories were replaced by protein, fat remained the same between the “Western diet” chow and the LC chow. It also appeared as though the diet was hypercaloric because the authors state that the LC rats were about a third more resistant to weight gain than other groups. So what they seem to have found is that when you overfeed proathergenic mice a high protein diet, they have greater atherosclerosis. They didn’t just vary the carbohydrate, they also significantly varied the protein with the LC chow getting 45% of calories from protein. In a human on a 2000 kcal diet, that would equate to about 200 g protein.
[PNAS 2009 Sept 8, 106(36) 15418-23]

His other statements and citations are directed against high protein. I haven’t read anything about the other two studies he cites [but one is his diet vs. Atkins vs. South Beach] so I’m currently in the dark regarding the definition of high protein in these studies. If it’s anywhere near the human equivalent of the PNAS study, I dunno, I can do significant carb restriction on a whole lot less protein than that.

Something I noticed today that may or may not be relevant. I tend to walk a lot faster now than most people I know. I always did when I was younger, but not “recently.” This is after about 5 weeks of the 6-week Cure. Is that an example of a metabolic advantage?

Speaking of the 6-Week Cure (If I may diverge a bit from the topic at hand): I seem to be shrinking (girth, weight), but my overall shape hasn’t really changed much since beginning. I still look the same in the mirror (at least, to myself). I’m guessing that this is due to losing visceral fat first, with the subcutaneous fat being left behind. If I’m right, my shape won’t change until the visceral fat is gone, and then my body will jettison the rest.

So Dr. Eades, to summarize, would you say that the insensible water loss is the reason why overall weight loss goes down, and the body’s increasing its insensible water loss gives the metabolic advantage? Just wanted to make sure I understood this. Thanks.

No, the insensible water loss is a surrogate for metabolism. As your metabolic rate increases, so does the rate of insensible water loss. And insensible water loss can be measured by accurate scales, which means that slight changes in weight due to insensible loss can be used to quantify metabolic rate changes.

Just a question, is insensible water loss really a surrogate for metabolism? I have the suspicion that it might not be as simple as that. Using a gross simplification (in the same vein as the bomb calorimeter simplification of calories) the end product of metabolism are the same as those of an oxydation. So at the end of reaction chain glucose and the fatty acid end as carbondioxid and water. If I use a reaction equation I can see that the combustion of glucose compared for example to caproic acid (hexanoic acid) yields the same quantity of CO2 and the same amount of water and using less oxygen for that. But the number of ATP (the energy currency) one gets out of it is less

I’m glad this is the last post debating AC, as I don’t think he’s worthy of your time, but I did enjoy the content very much. I had long wondered if the increase in protein or fat was the reason low carb diets satisfy us more and cause us to lose weight faster. The answer from the Kekwick and Pawan study seems to be “both”, with fat edging out protein (at least for weight loss).

Satiety remains a question in my mind; for me, the LC way of eating satisfies me, but it could be either the increased protein I’m eating, or the increased fat content. Fat seems to be the consensus, but a news article on primates led me to think perhaps a need for a minimum amount of protein might drive hunger (see http://news.anu.edu.au/?p=1213 … note the title, they may owe you a royalty).

Hunger. I think that is the most significant aspect of food and physiology.

Hunger was so strong, so unavoidable, so persistent, that the subjects of Ancel Keys’ semi-starvation study developed neuroses of varying degrees. One even went so far as to chew off a couple of his fingers. Their diet was about 1600-1800 calories per day of mostly plants with just a little bit of lean meat once in a while.

I will even go so far to say that hunger is an excellent measure of a metabolic advantage. Why? Because even while eating fewer calories, hunger is reduced on a low carb diet. If the reduced hunger is not the result of a metabolic advantage, then I don’t know what is.

I will even go further and say that hunger is what causes us to overeat, to grow fat, and all the rest. Don’t believe me? Simple question, why do people overeat? Simple answer, because they’re hungry. Why are they hungry? Because they don’t eat enough. I mean, isn’t that how it works for the rest of the world? I mean, I’m hungry because I didn’t eat enough. What about you? Right, but they overeat! Yes, they do. But what do they eat in fact? Or more appropriately, what don’t they eat enough of? The simple answer is that they don’t eat enough food.

Now I’ve lost you. I know, it’s quite a novel concept. Here it is. Is your body hungry for food or for something that isn’t food? After all, what you eat must feed you and satisfy your hunger. If what you ate didn’t satisfy your hunger, then what was it? It certainly wasn’t food, that’s for sure.

Let’s get back to Anthony Colpo for a moment. He said this in his book (I didn’t read it, it’s just a quote Dr Eades posted above):

“Given that protein and fat have been shown numerous times to exert satiating effects, while low-fat, high-carbohydrate diets (especially the liquid, low-fiber variety!) typically result in ravenous hunger, it’s not hard to guess during which diet the participants may have ‘cheated’ the most!”

That AC knows about hunger but fails to understand its significance is besides the point here. The point is that we know what causes ravenous hunger: High carb diets. A diet devoid of food will invariably cause hunger and cause us to overeat and ultimately grow fat. We might as well eat nothing and at least avoid all the consequences of a high carb diet except perhaps the hunger. Even then, eating nothing, as opposed to eating a high carb diet, will only cause hunger for the first few days after which hunger will subside and eventually disappear completely.

I have to wonder why Ancel Keys called his study “semi-starvation” study. But then I realized, people were starving as demonstrated by the emaciation and neurosis, yet they were eating a substantial amount of calories every day. It’s my belief that should they have eaten the same amount of calories mostly from fat instead of carbs, they’d have merely grown leaner yet remained in good health as when they started. A shame that Ancel Keys didn’t think to do that at the time. But never mind. Many a low carb adept knows how much satisfying low carb is. And none that I know of suffered the same fate as the Keys’ study subjects, i.e. emaciation. This means that if there is a metabolic advantage, hunger is an excellent measure, and emaciation is the caloric concequence of it. Because after all, when we lose mass, we lose calories.

The line: “(Scales that are sensitive to 2 g are extremely sensitive. Two grams weighs about three one hundredths of an ounce.)” seems to be in error. Two grams should be about 1/14 of an ounce, right?

Just got in after a 10 hour solo drive. Have to get up at the crack of dawn tomorrow to head for the airport for a hellish few days, so I haven’t had time to watch the videos. I will when I have time. But, I can tell you, someone will have to go a long way to ‘prove’ Popper wrong.

The guy in the video basically says that you can have a hypothesis that is scientific, yet cant be falsified, but can be proven.

He gives an example of a hypothesis that unicorns exist/have existed. You can’t falsify that, you cant go back in time and check everywhere in the universe, but, you can prove it by finding just one unicorn. So he says that the claim that science has to be falsifiable to be science is not correct, because there are scientific hypothesis that cannot be falsified, but only proven. He gives another example of a particle that has only one pole, which may or may not exist, so the theory of its existence cannot be falsified, but if you find one you prove it.

I haven’t seen the video, so I’m assuming your representation of it is correct. If so, then the guy has got is all wrong. The hypothesis that unicorns have existed is not a good hypothesis because it can’t be falsified. Just because no one can find one doesn’t mean they haven’t existed at some point. It’s impossible to falsify that hypothesis. The hypothesis should be stated thus: Unicorns have never existed. If stated that way, the hypothesis can be falsified by finding one single unicorn that has existed at some point in time. All Popper said, which people seem to have difficulty grasping, is that for an hypothesis to be valid, it must be stated in such a way that it can be falsified. That doesn’t mean it will be falsified, just that it can be if the right findings come to light.

All I am saying is that all that guy was saying is that you can have science that can’t be necessarily falsified that in reality is science that real scientists in reality are dealing with that is good. He gave a real example too, magnetic monopoles. Real scientists are right now actually in reality trying to be looking for looking them. You can’t falsify magnetic monopoles, because those real scientists don’t know how the magnetic monopole is actually in reality looking, so they might not be looking for real the right thing they think they may be looking for is not the one. So no falsifying, but you prove it when you actually found to be looking for one.

I tend to think of Popper as being, primarily, a philosopher of physics, conceived as a system of universal laws: “For all X such that Y, Z follows”. Universal laws cannot be verified, only falsified, and a host of philosophers who thought otherwise (Kant, Carnap) were wrong.

However, as you say, the demarcation line defining science surely includes statements of the form “There exists X, and here’s what we found”. The idea that the whole of science consists of universal laws has been a source of confusion.

“it’s not hard to guess during which diet the participants may have ‘cheated’ the most!” That’s almost a doff of the cap to low carb from Mr. Colpo. The metabolic advantage aside, if, as a low carber, I can eat food I like, without “ravenous hunger'”, and lose weight and feel healthier, that’s good enough for me. Thank you as always, Dr. Mike, for making pretty complex stuff understanable to those of us of a non-scientific bent. All the best. S.L.

Surely though there is a problem with your Popper reasoning; if all hypothesis should be falsifiable, and a study showing a metabolic advantage falsifies Colpo’s argument then surely at least one of his studies showing no metabolic advantage mentioned falsifies your position (if they dont then surely your hypothesis is unfalsifiable?). Either that or every one of his studies mentioned is poorly built.

No, it’s all in how one states the hypothesis. If the hypothesis is that there is no metabolic advantage, that’s a good hypothesis because it can be falsified. All that has to be done is show one instance of a legitimate metabolic advantage and the hypothesis is falsified. If the hypothesis is that there is a metabolic advantage, its much more difficult, if not impossible, to falsify. Why? Because all you can do is show a list of studies demonstrating that there isn’t a metabolic advantage, which doesn’t really prove that there isn’t. It may just be that no one has looked for one correctly. In the first example, all one has to do to falsify is find one legitimate exception whereas in the second example it’s impossible to falsify, which was Popper’s point. A valid hypothesis must be ABLE to be falsified. That doesn’t mean that it will be falsified, but as long as the hypothesis is structured so that it can be, then it’s a valid hypothesis.

Now I am curious. If you were someone, like AC, on the no-metabolic advantage “side” of the debate, how would you formulate your hypothesis such that it is falsifiable and/or satisfies Sir Popper’s requirements.

That’s the point. You don’t formulate your hypotheses to fit your own bias; you formulate them to seek the truth. If I didn’t believe in the metabolic advantage, I would still formulate my hypothesis thus: No metabolic advantage exists. This is a fine point that many people have trouble grasping. If I set my hypothesis this way: A metabolic advantage exists, it doesn’t work. Why? Because it can’t be falsified. I can search and search and never find a metabolic advantage, but that might mean that I just haven’t been looking hard enough or the equipment hasn’t yet been invented that allow me to find it or whatever. But that hypothesis can’t be categorically falsified. The other hypothesis, however, can, which is what makes it a valid hypothesis.

“Falsified” has the connotation of purposeful deception. Perhaps a better way of stating Popper’s reasoning is to say that a good hypothesis is one stated in a way that it can potentially be disproven.

Your description of this study was a really fascinating and well written account. I agree with you that just because the study is old doesn’t mean it was wrong or carelessly done. Some of those older studies are far superior to the modern ones IMO. Nowadays (well the last few decades), there are a lot of people trying to pursue very few positions in science, and told that they must publish, publish, publish. I’ve seen people get three data points and quickly draft a report for publication, without bothering to double check anything. If questioned, they said, if there’s a problem, just publish another paper correcting the mistake! Tenure track committees are said to “count better than they read”. And so I often feel that the older studies, done without haste and with greater attention to detail, are superior examples of science done properly.

I hope when you attack Ornish for his attack today on high protein diets, you acknowledge that he has been the leader in the media in pointing out the dangers of refined carbohydrates for thirty years, and that he (like you) loves to pick fights with people he sees as enemies, so exaggerates differences while minimizing points of agreement.

Thanks so much for this! The insensible water loss is a very valuable piece of the puzzle, and helps a lot. I try to explain to people how low-carb/high-fat means more nutrition in circulation (since insulin is not clearing it away), and higher mitochondrial activity, and that maybe their body temperature rises a bit as a result of a higher metabolic rate. But I never felt solid about the temperature rise. Now I see that the body temperature doesn’t have to rise, of course. The water loss goes up!
BTW, I’ve been reducing the protein powder content of my shakes somewhat, and increasing the fat, preferably coconut milk, or goat butter or goat cheese (for the MCTs), and it has broken me through another fat-loss plateau.

I found your analogy of the black swan very interesting. I’m somewhat feeling both you and Colpo are right. Let me explain my point of view.

It is very right that researcher should look more for a black swan than just finding more white swan. But, even if one black swan is found, and if only one is found, it still makes it an ”abnormality” that might have been there by random errors or strange circumstances. For the black swan to really be accept as something possible, we actually want more than one black swan. Otherwise, it’s still not very commun, and there’s good chance your never gonna see one in your life.

My point is, even if one or two studies found a MA, it could be dues to many reason, and not per se that MA exist. If it occurs in about every low-carber, it should be always easy to find it. Not only in 2 papers out of many. There has been other studies where they looked at the resting metabolic rate of people on low-carb, and they did not see any change.

You know how science work… it’s always the strength of the evidence that we must consider, not just only one or two papers.

Althought this post is very interesting and makes a good case, I don’t know yet what to believe, but what is sure is that most of the long term study to date find no significant difference in term of weight loss (althought we know that the diet tend to be about all the same in the end… so it’s not very reliable). And LC usually end up loosing a little more weight (usually mean 3 pounds)

But I still need more than one or two study to be convince that the MA really exist in about everybody going on a LC.

“…But, even if one black swan is found, and if only one is found, it still makes it an ”abnormality” that might have been there by random errors or strange circumstances. For the black swan to really be accept as something possible, we actually want more than one black swan…”

Come on! If you find just ONE black swan you have just proven that “No black swans exists” is false. Abnormality or not. If you are not sure that what you see really is a black swan then that is another story.

Just to make myself clear. The fact that one or two study show that there might be “black swans” around doesn’t make it THE NORM. We are asking here : is the metabolic advantage happening in about everyone going LC?” Is the the black swan common, not simply possible?

And the fact that MOST studies did not find a metabolic advantage should end the discussion right here, even if one or two study did find it. Anyone can cherry pick study to make his point, since there’s always contradiction in the litterature. It is the whole evidences that we must look at, and again, in this case, most study do not find a metabolic advantage – not the other way around.

This is exactly my point, and THE important point I think. It’s not about proving the calorie is a calorie is a calorie wrong or right, it’s about having the MA replicate in many other studies, which don’t happen. Why? Maybe because it’s not so common? Or something else?

Well, for me this is the only important thing anyway. Too bad if I missed your point Dr. Eades, this is the only one that I care about. If the Metabolic Advantage exist, it should be replicated always and easily. Otherwise, it just tell me not to count on it too much because it might never happen.

Thanks, Dr. Eades! You know how you can crack a walnut and the meat comes out in pieces? Nice, but you still wanted to see it come out in two nice halves? Well, your blogs are always like walnuts that come out in halves—satisfying on so many levels. 🙂

“Or, an alternative explanation is that, as with the Leibel study mentioned in my first critique, he either didn’t really read the paper thoroughly or he seriously misunderstood what he read.”

Who didn’t really read the Liebel paper thoroughly or seriously misunderstood what he read. Seems to be Colpo who got it all right…..

From Colpos response.

“Eades cites the data reported for subject 3, “a 55-year-old male with a BMI of 32, [who] maintained his weight on a high-carb formula at 2871 calories per day”. According to Eades, this subject “then required 3501 calories to maintain his weight on a 70% fat, 15% carbohydrate diet”.”

“OK, now I want you to scan all the way across to the column 2nd from the right, the one titled “Energy”. This column displays the actual daily energy intake of subject 3 in kilojoules (kJ). In other words, the actual amount of daily kJ subject 3 ate on each diet (to be doubly sure of this I recently emailed Dr. Jules Hirsch, one of the study authors, who indeed confirmed the figures in this column were the actual kJ intakes of the subjects). To convert the kJ figures to calories, simply divide them by 4.184.

As you can see, subject 3 ate 13,862 kJ/day (3,313 cal/day) on the 15% carb diet and 13,862 kJ/day (3,313 cal/day) on the 85% carb diet.

Now, scan your way back to the 4th column from the left, the one titled “Mean weight”. As you can see, subject 3’s mean weight during the 15% carb diet was 96.21 kg, and during the 85% carb diet it was 95.91 kg. So in reality, subject 3 ate the exact same number of calories on both diets and his mean weight during the two feeding periods was a bee’s cajone lower on the high-carb diet”

“So where on Earth did Eades get the figures of 2,871 calories per day for the low-fat diet and 3,501 calories on the low-carb diet? Where does he get off giving the impression that subject 3 “required” over 600 calories more daily to maintain his weight on the 15% carb diet?

Let’s go back to Table 1. Find the data for subject 3 again, and then scan over to the 8th column from the left, the one titled “Days on diet”. As you can see, subject 3 spent 23 day on the 15% carb diet, but only 18 on the 85% carb diet. Now, scan your way back over to the 5th column from the left, the one titled “WT INT*”. The figures in this column are the mean weights adjusted in light of the fact that the subjects spent different amounts of time on both diets. Using the daily weight data and the different durations of the diets, the researchers used a mathematical formula (shown on page 2 of the PDF) to calculate a “corrected” kJ intake. These are the figures of 12,016 and 14,652 you see in the far right column titled “CORREC kJ”. They represent the estimated daily kJ required for weight maintenance, calculated in light of the fact that the subject spent 5 more days on the low-carb diet”

“What would have happened when calculating the CORREC kJ figure if subject 3 had actually spent more time on the high-carb diet? We don’t know. What would have happened if, ideally, the subjects spent an equal amount of time on both diets? Again, the truth is that we don’t know.

What we do know is what actually happened: Subject 3 spent 23 days on a 15% carb diet eating 3,313 cal/day, and his mean weight during that time was 96.21 kg. He spent 18 days on an 85% carb diet consuming 3,313 cal/day and his mean weight was 95.91 kg”

“A l3-wk study of subject 12, first on 10% (75% CHO) of energy intake as fat and then on 70% (15% CHO)
of energy intake as fat. During both periods, 7322 kj per day were fed. Actual kj combusted were corrected, as described in Subjects and Methods, to 7468 kj and 6824 kj per day, respectively. It is notable that there was only 1 kg of weight variation during the entire study.”

I think it clearly states that subject 12 ingested the SAME amount of calories during both periods, which was 7322 kj per day.

Where does it says that the energy intake was adjusted so that there where different energy intakes dependent on diet composition?

There was small variations in weight during both the high carb diet and the high fat diet and the highest weight was actually seen during the high fat diet.

Another quote from the Liebel paper.

“There may be an interaction of diet composition and predisposition to obesity, with higher dietary fat content facilitating the expression of a more efficient metabolic phenotype (27). In this regard it is of interest to note that the three subjects (subjects 1-3 in Table 1) with highest BMIs had lower CORREC kj on the higher fat diets, whereas all but one of the other adult subjects had equal or higher CORREC kj on the higher-fat diets.”

In this quote you can read that subject 3 the 55 year old in discussion was one of the subjects that had the lower COOREC kj on the high fat diet.

If I look in Table 1 on subject 3 I can see that the ingested amount of energy on the high carb diet and on the high fat diet was the same, 13862 kj.

When looking at the CORREC kj for the high fat diet (70%) it says 12016 kj which is 2871 kcal.

When looking at the CORREC kj for the high carb diet (85%) it says 14652 kj which is 3501 kcal.

So how can you make the conclusions that the high fat diet required 3501kcal to maintaine body weight.

Dr.Eades: “One subject, a 55-year-old male with a BMI of 32, maintained his weight on a high-carb formula at 2871 calories per day. The same subject then required 3501 calories to maintain his weight on a 70% fat, 15% carbohydrate diet. Sounds like a metabolic advantage to me”

Also when you read this qoute from the Liebel paper again you can see that this statement above can’t be right.

“There may be an interaction of diet composition and predisposition to obesity, with higher dietary fat content facilitating the expression of a more efficient metabolic phenotype (27). In this regard it is of interest to note that the three subjects (subjects 1-3 in Table 1) with highest BMIs had lower CORREC kj on the higher fat diets”

“I am currently having this argument, vis-a-vis the Colpo/Eades exchanges, on a another forum I moderate!

In his dissection of chapter one of Colpo’s Fat Loss Bible the observation that one of the subjects in a study quoted by Colpo (to support his ‘calories count/no metabolic advantage’ stance) actuallyhad to consume more calories on a high fat, low carb diet to maintain his bodyweight at a constant level but had to eat fewer calories on a high carb, low fat diet to achieve the same goal. Colpo fired back that Dr Eades had misread the study data and that both diets had the same caloric value.

Colpo made the mistake of providing a link to said study and I discovered that Colpo was quoting the caloric value assigned to the diets at the start of the interventions while Dr Eades had correctly quoted the caloric values as adjusted during the intervention to correct for changes in bodyweight!

Further, if you look at all of the subjects in the various dietary interventions, most had disparate caloric intakes on both low carb/high fat and moderate-to-high carb diets in order to maintain a stable bodyweight. Now it seems to me that, for a study that Colpo is using as evidence for his contention that it is calories only that count and there is no metabolic advantage (or disadvantage) from varying the macronutrient composition of said diets, the data, for the most part, seems to indicate the exact opposite!”

I am sorry, to me it is rather ridiculous. It seems this criticism directly shows that one of your claims was wrong, and you might have misread the studies. You just keep on saying read my post and read the papers, presumably until we all start agreeing with you. Why not just answer the criticism, instead of avoiding it?

From the paper “Energy intake required to maintain body weight is not affected by wide variation in diet composition
Am J Clin Nutr l992;55:350-5.” , attached by Eades in the previous blogpost.

If you take a look at Fig.1 and then at the text under it, it says.

“A l3-wk study of subject 12, first on 10% (75% CHO) of energy intake as fat and then on 70% (15% CHO) of energy intake as fat. During both periods, 7322 kj per day were fed. Actual kj combusted were corrected, as described in Subjects and Methods, to 7468 kj and 6824 kj per day, respectively. It is notable that there was only 1 kg of weight variation during the entire study.”

I think it clearly states that subject 12 ingested the SAME amount of calories during both periods, which was 7322 kj per day.

Where does it says that the energy intake was adjusted so that there where different energy intakes dependent on diet composition?

There were small variations in weight during both the high carb diet and the high fat diet and the highest weight was actually seen during the high fat diet in subject 12 by looking at Fig.1

Another quote from the Liebel paper.

“There may be an interaction of diet composition and predisposition to obesity, with higher dietary fat content facilitating the expression of a more efficient metabolic phenotype (27). In this regard it is of interest to note that the three subjects (subjects 1-3 in Table 1) with highest BMIs had lower CORREC kj on the higher fat diets, whereas all but one of the other adult subjects had equal or higher CORREC kj on the higher-fat diets.”

In this quote you can read that subject 3 the 55 year old in discussion was one of the subjects that had the lower COOREC kj on the high fat diet.

If I look in Table 1 on subject 3 I can see that the ingested amount of energy on the high carb diet and on the high fat diet was the same, 13862 kj.

When looking at the CORREC kj for the high fat diet (70%) it says 12016 kj which is 2871 kcal.

When looking at the CORREC kj for the high carb diet (85%) it says 14652 kj which is 3501 kcal.

So how can you make the conclusion that subject 3 required 3501kcal to maintaine body weight on the high fat diet based on the Leibel study you refered to in the other blog post?

Not that it has anything to do with your tyypically fine performnace here, but I beleive that it was William James who said, “”If you wish to upset the law that all crows are black, you mustn’t seek to prove that no crows are; it is enough to prove one single crow to be white.”

I didn’t realize William James made that point. Sir Karl Popper made it famous, though. At least as applied to swans. Swans are a perfect example because everyone thought all swans were white until black swans were found in Australia.

Here’s my angle; I want to find that black swan, because I don’t want to prove all swans are white, I want to know WHY all swans are white, and while finding a black swan may marr the perfection of the white swan theory, it is far too valuable for the clues it can give as to why MOST swans are white to be ignored.
Transpose this to my favourite field, antioxidant/free radical theory, where the black swan is the CARET study.
Why aren’t more people interested in the WHY of that result?
Do some free radicals, in very high concentrations (as in a smoker’s lung), actually quench each other (Petkau effect), so that inadequate or too narrowly specialised antioxidant supplementation can actually remove a partial antioxidant effect of high-dose free radicals?
Do UV blocking antioxidants reduce vitamin D conversion?
Does the all-cis beta-carotene used in the CARET study reduce the absorption of other carotenoids, tocopherols, and some flavonoids? (the answer is yes, more so on a low-fat diet)
Did the dosing schedule used (only every second day) allow oxidised carotene to outbalance reduced carotene for long periods?
Explaining the black swan successfully can validate a modified white swan theory, as well as disproving the original version (i.e. all antioxidants are always beneficial in all circumstances). Surely this is the only way forward in science, which ought never to be trench warfare where one tries to win by attrition, blockade and propoganda, but a war of intelligence gathering, sudden incursions and breakthroughs.

I think Anthony knows that Gary Taubes’ case against the classic caloric model of obesity is extremely strong.

The caloric model is a theory born of logic alone and completely ignores the follwing data:

* worldwide epidemic of obese 6 month olds

*extreme poverty and malnutrition going hand in hand with obesity.

Anthony has NEVER rebutted Gary Taubes excellent criticisms of the failure of the classic caloric model of obesity. Anthony simply restates the hypothesis as if that takes care of it. It doesn’t- not by a long shot. Or he will call Gary a “retard”. For a guy who brags about how intelligent he is, like Anthony routinely does, that certainly is not that bright.

Anthony just does not understand that obesity is ungodly complex. Obesity is a serious , chronic medical condition of fat cell disregulation. Perhaps we can suggest to Anthony to type into Google the following phrases ?

Hi Mike – we saw two black swans this past spring on the fens in England. Maybe the Aussies have shipped the black ones back to get even w/ England for shipping convicts forward? Just a joke. Just barely. But the swans were amazing.

Thanks a mill for the column. You do make science and reasoning accessible and applicable to life. Good work!

..actually a real good example is whats happened to Toyota of late.
Imagine if its a computer programe.. maybe something deadly small but its caused a whole body of evidence i.e Toyotas are wonderfully reliable (i tried driving a little Tazz in Damaraland) to be over turned.

And i think i’m right in saying Taleb didn’t invent the black swan just popularized it oops just read the above.
I’d read it was John Stuart Mill (on half a pint of shandy was particularly ill) invented the concept..but what do i know ?

> The easy way to bolster their hypotheses is to continue to tally up all the white swans they find and forget about looking for black ones.

And, when they find a black swan, they say something like this: What appears to be a black swan is actually a white swan with severe health problems, which supports our original assumption that no naturally occurring black swans exist. These results call for treatment of any white swans that show signs of what we term here “black swan syndrome” with preventive doses of [the drug manufactured by the company funding the research].

1.) I’m surprised how much trouble both you and AC will go through debating a metabolic advantage of supposedly 100-300 calories. You both probably burned more calories debating one another than a metabolic advantage will ever get you (ok, I realize that’s not true over the long term, but just saying you both put in a lot of effort for a rather small component of a diet). but i did learn a lot.

2.) I’m always struck that trainers seem to think they are experts in nutrition, medicine, and anatomy.

3.) You mentioned amphetamines raising metabolism, and subsequently, water loss. Does this perhaps partly explain the “dry mouth” symptoms that those on ADHD medications experience?

4.) Any thoughts on raw milk? I know it’s fairly carby, but seems to me the impact may be blunted during digestion, and it may be one of those carb sources that is well worth it for the nutritional value. Are you a W. A. Price supporter?

I tried using your ‘contact’ button to ask this question, but it didn’t work, so I’m afraid this is off topic from your post.

I was wondering if you could write a post regarding pregnancy and low carb. Specifically, the fact that many doctors, even Dr. Atkins said that pregnant women should not be in ketosis during pregnancy. However, my logical mind has some questions:

1. There have been reports in the news lately regarding advising obese pregnant woman to diet while pregnant (not any specific diet). If dieting is bad overall, then why advise obese woman to diet?

2. Ketosis is bad for pregnant women/fetus. Hmm, the first trimester comes with varying degrees of morning sickness for many, and the end result of that could be ketosis in many woman, not due to lowcarbing specifically, but due to not eating, eating sparingly, or throwing up what is eaten. Makes me wonder if ketosis is really bad.

3. Inuit woman, who eat basically an all meat diet, get pregnant and have babies….umm…

Please note that I’m not suggesting that normal weight women go on a diet! What am suggesting is that a lowcarb diet where you may in fact be in ketosis is not a harmful way to eat during pregnancy.

My opinion on diet and pregnancy is that the mother should avoid a high-refined-carb intake during the first trimester. That is the point at which the developing fetus is laying down its pancreas and entire metabolic system. If the mother is constantly spiking blood sugars, some research indicates that the fetal pancreas suffers. The baby may be born slightly insulin resistant.

During the third trimester the mother should consume a ton of protein because that is when the fetus is growing at its most rapid.

Check out the forum ” IF and the childbearing woman ”
over at the PaNu website.
Quite an in-depth discussion of that very topic. jerome, TxRain, et.al. cover it pretty well from a layman’s standpoint, and Dr. Harris referees.

Doctor Eades, every great man deserves a pass for one major flaw. For you, that appears to be a low taste for street-brawling with bullies. I use the term great with some trepidation, not to embarrass you, but after considerable time spent reviewing your writings and your impact on the ongoing revolution in nutritional understanding.

I’m very impressed with your guts. Anthony Colpo is no pushover; he’s brilliant, combative! and a no-holds-barred brawler. Win, lose or draw, you guys put on a hell of a show. An onlooker had to enjoy the pure theater of the clash between the no-nonsense gentleman and the total asshole bad guy, played with relish and skill by Colpo.

For what it’s worth, I’ve expressed myself elsewhere about the advisability of this battle; still, I have to admit you two appeared to be having fun, and certainly a great many people were entertained.

My purely selfish take on all this is that you’ve got better things to do with your time. Hell, maybe Colpo does too.

I’m well along in years and I’m looking forward to reading as much of your insightful and valuable writing as possible.

I’ve got a low taste for a lot of things; this is just the only one you know about. 🙂

Not to worry, though, this is my swan song in dealing with Anthony Colpo. No matter the provocation, I’m through with it. There are plenty of words out there from both of us, so readers can decide for themselves who is the more correct.

Very enlightening post. I love the white swan – black swan analogy. It has wide applications beyond this post. Seems that most medical “science” these days is nothing more than parading the white swans while denying/suppressing the existence of black swans.

So observing that there is a metabolic advantage isn’t a hypothesis, it’s an observation?

Leptin causes bone precursors to differentiate into osteoblasts, rather than adipose cells. Looks like energy source makes the decision, to me, leptin acts to encourage fat metabolism in much the same way that insulin works on glucose metabolism. Maybe it works through mitochondrial decoupling? ROS as signalling molecules? This connects to vitamin d’s role in both energy metabolism and cell differentiation. It might also explain why even very brief periods of bone loading are so protective against bone mass loss; even a brief burst of ROS might result in a whole crop of precursor cells being steered in the right direction.

If ROS is the determining factor in differentiation anywhere in the fetus, I don’t think it’s possible to underestimate the importance of good blood sugar during pregnancy.

The rampant cheating in the Kekwick and Pawan study could very well explain the differences. The Rabast studies have been discussed already, and glycogen loss and/or loss of lean tissue could be the reason of the differences.

Those two studies should be looked upon as anomalies, for the reasons mentioned by Colpo.

If there was a metabolic advantage other scientists should have been able to reproduce these results. Fact is no one has been able to.

Fact is there are more 24 ‘white swans’ and none of them have been able to find a metabolic advantage. Out of 26 metabolic ward studies, only 2 have shown a metabolic advantage. How can that be explained away?

Lastly, metabolic ward studies present the best scientific proof we have when we study nutrition. No other environment provide better control. To dismiss them like Eades does seems just… strange.

You can’t apply the one black swan claim to anything. A good hypothesis based on your standards regarding saturated fat is that saturated fat does not cause heart attacks. Now, some studies have shown that increasing saturated fat increased heart attack rate, like the Finnish Mental hospital study. One black swan out of like, what, 14 white swans? Why don’t you apply the logic here? Because it suits your bias?

Now, I know it was a badly designed study and an anomaly. That’s what you would say. But when 2 out of 26 show a metabolic advantage, you run around telling it only takes one black swan.

We should let the readers know that only 2 out of 26 metabolic ward studies showed metabolic ward. You can’t hide behind the black swans from this data. Due to metabolic advantage the black swans aren’t fat and we can see you right behind them. You go off with wild speculation why they didn’t show, some had too few calories, some must have cheated etc, but saying that in those 2 studies something was wrong, it was water/glycogen loss or chance or something else (perhaps the high carb group cheated more? certainly more plausible than your claims in your last posts that the low carb group cheated to account for the metabolic advantage), you say another “non understander”.

“If there was a metabolic advantage other scientists should have been able to reproduce these results. Fact is no one has been able to.”

26-24=2

“2 have shown a metabolic advantage”

“Fact is no one has been able to” != “2 have shown a metabolic advantage”

So didn’t you admit it was reproduced at least once?

I think I understand now.
It’s because 24 is bigger than 2!
Oh I forgot colpo said ignore the man behind the curtain (i.e. the 2 studies that showed it are anomalies).

Have you read the studies or just the abstracts? I have been very surprised by how many times the abstract of studies seems completely different from the actual study data. The point of the swan story is a single “anomaly” could change the entire game.

Instead of all this theoretical masturbation (which probably burns quite a few kcals producing a Metabolic Advantage 😉 ) why don’t you get yourself a Bodybugg/GoWear Fit, strap it on and see how many kcals you’re burning. Then eat loads of fat and tell us what happens.

I read this Gardner piece when it first came out and disagreed with it then. I reread it a bit ago and still disagree with it. David Stove, one of my favorite philosophers, also wrote a piece critical of Popper, which I disagreed with, but it was clever writing and good reading.

The fact that Popper had human failings shouldn’t detract from his work.

I agree that science moves forward by inductive reasoning, which is basically finding one white swan after another. Popper realized that and said that, as a consequence, an hypothesis can never really be proven. But if it is falsified, it can be disproved.

You once had a link to a farm (in Virginia?) where they rotated the animals feeding on the land–like chickens first, then they moved them out and moved in pigs or cows or something–and the idea was a really sustainable organic kind of farm. Do you remember where that was on-line? (If you can even understand this rambling inquiry I’ll be amazed–I’d just like to find that link again.) Thanks for all you do.

Dr Eades, I’m intrigued by the use of Popperian falsifiability in defending your position. Please understand that I have no position in the metabolic advantage battle – I’m interested in how you’re using the philosophy of science, given that people in the nutrition wars rarely do so. Without further ado…

You claim that all it takes is a single observation of a black swan to disprove the hypothesis “there are no black swans”. This is true – but only if the observation of the black swan is well justified. Merely seeing a black swan does not answer the basic epistemic question of how you know you saw a black swan, or more importantly, how others can know that you saw the black swan.

To use a modern analogy: I posit that there are no Bigfoots on Earth. Many people claim to have observed a Bigfoot, but until I see some sort of testable evidence to that effect (the capture of a body that many can examine and verify that it is a bigfoot) the claimed observation does not disprove my hypothesis. It may be knowledge in a sense, but it hasn’t been justified.

Falsification is how science establishes knowledge – proof by contradiction, essentially. But repeating an experiment is how science establishes an epistemic justification, how it shows that the falsification was actually valid, which is just as important. In your argument you have focused on the observation of the black swan as adequate to show that there are black swans, but I’m not sure that you have covered your bases when it comes to justifying that black swan was actually observed. Without confirmation by other researchers, any one result could very well be just another Bigfoot sighting.

I recognize that you have limited yourself to AC’s paper selection in forming your argument, which leaves you limited in your ability to find repeat observations. This probably explains why you are focusing on a single black swan sighting and avoiding the repeatability aspect of scientific knowledge. So perhaps this whole comment is just another non sequitur – apologies if so. In the end, though, one cannot ignore justification, and so it always takes more than a couple of Bigfoot sightings to establish Bigfoot’s existence.

Thanks for your time and blog – I’ve been reading for a while but haven’t commented before. I appreciate the work you put in (just to have snarky people like me take potshots at something you probably didn’t want to talk about!) and look forward to your next posts.

Thanks for the thoughtful comment. I agree with you that it takes more than an anecdotal sighting of Bigfoot to prove his existence.

I was limiting myself to Colpo’s papers, so I had to use only those he discussed. There are many other papers out there showing a metabolic advantage and the 2nd Law of Thermodynamics almost demands a metabolic advantage. To find a metabolic advantage, you’ve got to look for it. Most of the authors of the papers Colpo used weren’t looking for a metabolic advantage, they were looking for something else.

The body has glucose demands that must be met. If these demands are met by dietary carbohydrate, the energy requirements are almost nil. If the glucose demand has to be met by gluconeogenesis, i.e., the conversion of protein to glucose, the stripping of glycerol from fat and it’s conversion to glucose, and a few other cycles that provide glucose, more energy is required. Since a low-carb diet provides very little carb, the increase energy required for the processes to synthesis glucose consume more energy, which implies a metabolic advantage to such diets.

It appears that Anthony Colpo has shut his site down ? (or at least I can’t access it)

Hopefully ,Anthony and his like minded followers will see there is far more to obesity than calories. It is ungodly complex.

I hope Anthony sees that the key is in the behavior of fat cells ,their dysregulation and how and why they are in a lipohylic state and how to jolt them out of it. ( Starvation and semi- starvation is not the solution, terrible for our health and will cause organ, bone and muscle loss) So much for the calorie theory dogmatists……..

It’s a shame Anthony can’t be on Gary’s side and help the both of you expose the cholesterol scam. That would of been the most productive thing Anthony could have done. It’s a shame that he has changed.

You, Gary Taubes, Dr. Robert Lustig and blogs like Matt Metzgar’s are the future for understanding obesity.

The dogs may bark but this caravan has moved on. This debate is over. Those who dogmatically refuse to recognize the variable effects of different types of food calories should be consigned to the rubbish bin of science. They are the defenders of what has consistently failed. What they advocate does not produce any favourable outcome. They have had ample opportunity to demonstrate their hypothesis and come up short.

Except for shooting fish in a barrel for demonstration purposes it’s a waste of time to converse with the close minded. Stay the course Dr. Eades.

Thank you for your thoughtful article on this topic, I have been doing my best lately to absorb information relating to a low-carbohydrate diet, and this article gave me a lot to chew on. (pun intended)

I felt that the evidence you presented here, especially regarding the rigor and results of the Kekwik and Pawan study did a wonderful job of rebutting the criticisms aimed at it, and clearly showed that it was far from a ‘poorly controlled mess’.

However, I felt that the analogy of the ‘black swan’ was used to rebut some points in a way that was not justified, although I certainly am not in disagreement with the logical principle that one counterexample falsifies a hypothesis. There is one particular user comment and your answer that I want to address first because it’s a bite-sized start: Your reader makes a comment about “24 ‘white swans’ vs. 2 ‘black swans'” to which you give the correct answer, that it only takes one black swan to disprove the hypothesis. However, the issue (which I hope to make clear in more detail following) is that people are trying to make a valid point, but since the swans analogy doesn’t provide an easy way of stating the point, it gets lost in translation.

The point is this: when studies of this type are performed, it is necessary that the same test give consistent and reproducible results when performed by independent researchers, and in order to be accepted into the mainstream, will likely require many independent verifications of the results. Such results must be both consistent and reproducible, in other words it is not just required that the same test give the same result sometimes, but that the same test give the same result a very high percentage of the time, within some reasonable error margin to account for methodology mistakes and other possible issues or subterfuge.

In swan terms: the same swan (a sufficiently similar experiment being run) needs to test black (return the same results) in many independent attempts to demonstrate it’s blackness (independent verifications of the same experiment.) I think the author of the 24 vs. 2 comment I mention above was just finding it hard to overcome the swan analogy’s limitations. Rather than the idea being that 26 separate swans were examined, and 2 black counterexamples were found, the idea is that 26 (assumed to be sufficiently similar) experiments were run (26 tests of the same swan), and the great majority of those attempted verifications did not obtain the same results (24 of 26 tests did not show that the swan was black) so the original experiment’s results (the swan being black) were not confirmed by independent investigation, and therefore are not acceptable as a counterexample. (Whether the 26 experiments are sufficiently similar, I do not know, but I believe that was the assumption being made.)

My basic issue is that, while the ‘black swan’ clearly illuminates falsification through counterexample, it does not address (at least without further development) the sometimes quite complex issue of demonstrating that something actually *is* a black swan. Even in this seemingly easy-to-prove case; i.e. that a black swan has been found, a little though-experimentation shows it’s not as clear cut as one might initially think.

For instance, what should be accepted as an adequate demonstration that a particular swan has been found that is a black swan? Is it good enough for one person to claim to see one? A hundred? If it’s merely eyewitness accounts (maybe black swans are very hard to catch), do you need to make a judgement based on the number of sightings, and possible ulterior motives of those who report having seen them? Or, maybe, this could never be enough, and you would need photo or video evidence? But, wait, photos and videos can be doctored; so perhaps a number of photos or videos from a number of disinterested people? Or, no, because is it possible that someone is taking white swans, somehow coloring them black, and then taking them to areas they know that tourists with cameras are likely to be? So, maybe a research lab would have to actually catch one and perform tests on it to make sure it’s not just a doctored white swan? Hmm, but one lab could mess up the tests, or be deceptive, so perhaps you have to provide a lot of labs access to it? In fact, wouldn’t it be ideally quite a few, in order to eliminate the possibility of collusion? So, if a significant numebr of independent, well-respected labs tested it, and they all decided it was truly a black swan, then don’t we finally know for sure we have our counterexample black swan?

But, wait! Even at this point, we aren’t really justified in making a statement that strong. Really, it seems like the strongest statement that would be scientifically justified is: the current scientific consensus is that there is at least one true ‘black swan’. For instance: imagine someone had researched and discovered all the existing tests that labs were equipped to run, and colored a white swan using a method that none of those tests would detect. Still, if further testing many years later brought to light the old deception, the new scientific consensus would once again be that no black swan was yet found.

Ok, I know I was probably just beating a dead swan there by the end. But it serves as the backdrop for my point: as hard as it could be to get a fairly solid scientific consensus on something that is (seemingly) just a matter of looking, it will only become more difficult as the verification process becomes more complex.

One of the ‘swan’ analogies in your article is as follows:

“In other words, AC is saying: that black swan over there isn’t really a black swan, because all the other swans I’ve pointed out are white. And since all the others are I’ve pointed out are white, that one can’t be black. It’s impossible.”

I find this the best example in the article of the results of oversimplification due to use of the ‘swan’ analogy. When I read the meat of his objection (“For a research finding to be considered valid, it must be consistently reproducible when tested by other researchers. […] [T]he findings by Rabast and colleagues fail dismally on this key requirement.”) it seems clear to me that he never admits that that swan ‘over there’ is black, and his argument for that position has nothing to do with the number of white swans he’s seen, but instead he denies that whatever results showed the ‘over there’ swan to be black are not consistently reproducible by other researchers (i.e. have not become a part of scientific consensus on the matter).

I think a more charitable restatement into ‘swan form’ would be something like ‘this study showed this swan to be black, however no scientific consensus has been reached verifying the result, and here are some studies of the same swan that indeed did not reproduce the results.’ And, although I can see perhaps arguing about whether the other tests he points to have been performed in a similar enough manner to qualify as testing the ‘same’ swan shown to be black by the first study, it seems to me perfectly valid to pointing to the other studies that he believes demonstrate a lack of reproducibility. Whether the other studies are looking at the ‘same’ swan is up for debate, but I definitely see no evidence in his statement that he thought these studies were studying a lot of different swans that turned out to be white, and much to indicate he thinks they were all studying the same swan.

Furthermore, as far as I can tell, even if you can show that all his other studies are of a different swan, it doesn’t impact his argument. Even if zero other studies of the ‘same’ swan have been done, it still is not possible to claim a scientific consensus that a ‘black swan’ has been found, since one of the hallmarks of the scientific method is that, before a result is accepted as valid, others must have been able reproduce the results. At best, in this case, you could state something like “one study has been reported to show that a ‘black swan’ has been found, however the results have not been independently verified.” (Unless of course you have a lot of other studies of the same swan that do offer independent verification that the original conclusion is valid.)

In the same vein I believe the ’50 year old study’ objection to fall in the same category; it’s not that he believes the age of the study is it’s sole fault, it’s the fact that none of the other studies of the ‘same’ (in his opinion) swan since then have verified the original conclusions.

So, this is more of a tome than a comment, although I hope someone finds it interesting or useful. I do not know the details of any of the other tests that were run, but I would be interested to see some results of any faithful duplications of the original experiments that showed a metabolic advantage, since ‘identical’ may be the only test that is ‘sufficiently similar’ to gather the same results. And, of course, if I’m way off base in my examination of the issues here, I’m eager to learn where I went wrong.

I understand your argument completely. And I agree to a certain degree. I limited myself to the papers that AC used to ‘prove’ his point, so I couldn’t bring in other black swans to add to the total.

I spent Part I of the two part critique demonstrating that most of the swans AC claimed were white were actually gray at best. And I showed that the two black swans he blew off were really black swans. The two black swan studies were designed to actually look for a metabolic advantage. Most of the 24 studies AC mustered to disprove the metabolic advantage were not designed to look for one – they were designed to look for something else. Several of them did show a trend toward a metabolic advantage, which is why I felt the preponderance of the evidence tended to demonstrate a metabolic advantage.

The Keckwick and Pawan study was such a meticulous study done specifically to look for a metabolic advantage that I consider it a true black swan. There are other studies that show the findings and some that don’t. But, theoretically, there should be a metabolic advantage to these diets, so finding them shouldn’t be a big surprise.

Regarding the Keckwik and Pawan study it is not difficult to understand why the subjects didn’t lose any weight and even gained weight on a carb-based diet as opposed to the fat- and protein-based diets when you know what effect carbs have on the retention of water.

If you look in the paper and fig 8 you can see that at least in three subjects the carb diet was preceded by the protein- and fat diet without any stabilization period between the different diets.

The same can be seen in diet of series 3 switching from a the high fat diet to a carb diet without any stabilization period.

I find it hard to belive that it wasn’t anything else than the water and weight retaining effects of carbs switching from a fat based to a carb based diet that was seen in the Keckwick and Pawan study.

“Observations on the effects of carbohydrate on water balance are hardly new. In 1769, William Stark (2) recorded a weight gain of 8 lb. in 5 days after changing his diet from meat to flour. This phenomenon of rapid weight change with alterations of diet composition was confirmed by Bischoff amid Voit (3) in 1860 and Bemiedict amid Milmier (4) in 1907.
Another line of experimental evidence on the role of carbohydrates in relation to water and electrolyte balance was initiated by studies of fasting, which in effect is a low carbohydrate diet at the cellular level. In 1909,
Hammarsten and Mandel (5) pointed out that during fasting “the body loses more water than is set free by the destruction of tissue.” Benedict (6) in his classical studies on the faster, Levanzin, demonstrated that early in the fast, weight loss exceeds that which can be explained on a caloric basis. This was attributed to a change in water
balance.”

“Individual tests with salt, protein, and fat, or carbohydrate demonstrated that only carbohydrate produced salt retention and its associated water retention during refeeding of the previously fasting patient. These results were confirmed by Wright, Gann and Albertsen in 1963 (15) who found sodium and water retention after glucose administration to fasting subjects.
In 1965, Rapoport, From and Husdan (16) had similar results on refeeding of fasting subject”

“Addition of 50 g of glucose to the formula isocalorically replacing fat resulted in prompt retention of sodium (in one instance within 2 hr) and cessation of weight loss.
The weight and salt loss on the carbohydrate free, salt containing diet was indistinguishable from the formula, salt free diet. These findings demonstrate that the earlier reports of weight loss in excess of caloric balance in fasting were the result of the limited amount of carbohydrate in the metabolic mixture rather than the absence of exogenous calories”

Here is a study much better performed than the Keckwik-study because they actually had a mixed diet before and after each diet to prevent any carry over effects from the preceding diet. And actually had the subjects on the same amount of days on each diet, 10 day, as opposed to the Keckwik-study 5-9 days??.

The results. Greater weight reduction on the ketogenic diet but not greater fat loss.

Composition of Weight Lost during Short-Term Weight Reduction
METABOLIC RESPONSES OF OBESE SUBJECTS TO STARVATION AND LOW-CALORIE KETOGENIC AND NONKETOGENIC DIETS
The Journal of Clinical Investigation Volume 58 September 1976-722-730

“On admission, each subject was randomly assigned to one of six experimental schedules as shown in Table II. Each schedule embodied three 10-day regimens: starvation, an 800-kcal per day ketogenic diet very low in carbohydrate content, and an 800-kcal mixed diet that provided carbohydrate and fat in conventional proportions. To minimize possible order effects, the dietary regimens were imposed in counterbalanced sequence across subjects. Also, a 1,200-kcal mixed diet was provided for 5 days before and after each experimental diet to reduce possible carry-over effects from the preceding regimen.”

“On the 800-kcal ketogenic diet, subjects lost (mean+SE) 466.6 ±51.3 g/day; on the isocaloric mixed diet, which provided carbohydrate and fat in conventional proportions, they lost 277.9±32.1 g/day. Composition of weight lost (percentage) during the ketogenic diet was water 61.2, fat 35.0, protein 3.8. During the mixed diet, composition of loss was water 37.1, fat 59.5, protein 3.4. The mean quantity (granms per day) of fat lost during the ketogenic diet was 163.4; during the isocaloric mixed diet, it was 166.7. Mean protein loss (grams per day) during the ketogenic diet was 17.9; during the mixed diet, it was 9.5.”

“The findings demonstrate that, over a 10-day period, the energy value of body constituents lost during adherence to an 800-kcal diet is minimally affected by wide variations in the proportions of fat and carbohydrate ingested. Discrepancies in rate of weight loss induced by ketogenic vs. nonketogenic isocaloric regimens result almost entirely from differences in water balance. Rate of fat loss is a function of degree of energy deficit.”

Where are the figures for waterretention during the carb-based part of the diet series 2?

Were are the figures for fat loss during the fat-, protein-, and carb-based part of the diet 2 series?

As you can see in the paper

Composition of Weight Lost during Short-Term Weight Reduction
METABOLIC RESPONSES OF OBESE SUBJECTS TO STARVATION AND LOW-CALORIE KETOGENIC AND NONKETOGENIC DIETS
The Journal of Clinical Investigation Volume 58 September 1976-722-730

there was weight gain when switching from a ketogenic diet to a mixed diet but still a net fat loss due to a negative energy balance. The weight gain was from water.

“During the 5-day 1,200-kcal postexperimental periods, weight gains occurred after the 800-kcal ketogenic and
fasting periods, and weight losses were measured after
the 800-kcal mixed diet (Fig. 4). In the postexperimental
period that followed the 10-day fast, the rate of weight gain averaged 145 g/day. During this time, water was being retained at an average of 271 g/day, fat was being lost at an average rate of 127.9 g/day, and protein was being retained at an average of 1.9 g/day. These data show that the weight gain during the postfasting period was due principally to water retention, a process that occurred even while net fat loss was continuing A somewhat similar situation obtained during the 1,200-kcal period that followed the ketogenic regimen. After the ketogenic diet period, there was some
weight gain (52.0 g/day), also attributed to excessive water retention (180.6 g/day), in the face of continuing fat and protein losses (125.9 and 2.7 g/day, respectively).”

Where can I find figures for this waterretention in the Keckwik-paper when switching from the highfat-diet to the high-carb diet during diet of series 2?

“Table v shows the losses of body-weight and bodywater in patients on the highfat and the high-protein diets. The
high-carbohydrate diets are excluded because changes in
body-weight and body-water were negligible during this period.”

No figures for WATERRETENTION during the high-carb part of diet of series 2.

No data was presented for the high-carb diet because there was no weightLOSS seen and no mention about any waterretention even though it could be seen there was gain in weight from water.

From Colpos latest answer: “However, they did present the overall water loss data for twelve patients on the 1,000-calorie diets (Table IV). Again, there is wide variation in the amount of total body water lost, and there are two individuals who despite losing 1.8 and 3.6 kilograms of bodyweight gained 0.8 and 0.5 litres of body water, respectively. Because no increases in body water were observed during the low-carb diets, this increase in body water obviously occurred during the high-carb phase of the 1,000 calorie experiment”

And maybe you could learn something from the Danish researchers Olesen and Quaade.

“The fact that Kekwick and Pawan’s obese patients temporarily maintained their weights on high carbohydrate diets yielding as little as 1000 calories (which is decidedly lower than the basal metabolism of a euthyroid adult) while others lost weight on high-fat diets containing as much as 2600 calories, seems to us to be the best indirect argument against Kekwick and Pawan’s main premise—namely, that the proportion of water in body-weight is unchanged. Their data reveal, not surprisingly, that some patients lost considerably less than the average 30-50% of the weight loss, while others augmented their total body-water content despite weight losses of up to 3.6 kg. In some the loss of water was much greater than the average, and in a few the water loss exceeded the loss of body-weight. This can only mean that the method of determining total body-water was too inaccurate to allow safe conclusions regarding fluctuations in bodily-fluid during short observation periods”
Fatty Foods and Obesity. Lancet, 14 May 1960; 275 (7133): 1048-1051.

Why don’t you have anything to say about the Yang study with its much preciser measurments, which clearly shows that even if you gain weight when switching from a ketogenic diet to mixed diet you are still loosing fat tissue and the weight gain is due to waterretention?

You actually think this didn’t happen i the Kekwik study? It surely did and the data actually confirms it.

And you didn’t answer this question:

Were are the figures for fat loss during the fat-, protein-, and carb-based part of the diet 2 series?

You didn’t answer because you can’t. They didn’t measure fat loss in the Kekwik study unlike in the Yang-study where you can find figures for fat loss.

Dr. Eades,
Great post as always. Just a note on what I think is a typo: in the paragraph that begins “If you breathe on a mirror…”, the next 3 instances of breathe/breath are switched. I think it should read “…water vapor in your breath. This vapor is water that you lose every single time you take a breath. You breathe approximately…”

No need to publish this comment, just thought you might want to know. Thanks for all your good work.

Was also just reading TC Cambell’s review of the new Atkins book on Amazon. Those two have a lot in common, haha, waffling on irrelevantly and irrationally and endlessly.

His original point was that the metabolic ward studies were absolute proof that there is no met. adv. My only question, way back when, (and again, sorry I asked, really) was, izzat true? Or is it a question of how you interpret said studies?

He contends the studies can only be interpreted one way, his way. And he defends that position with a great load of, cough cough, interpretation. Whether or not MA exists, he loses the argument right there.

I’m glad you mentioned Campbell’s book because I’m also working my way through it, but I forgot to put it in my list in the current blog (I probably repressed it). I figured if I was going to critique it, I ought to read it. I also sprang the $200+ for the original China Study, which refutes a lot of what he writes in the popular book.

You are still not answering my questions or statements. So one more time.

Page 158 Kekwik

“Table v shows the losses of body-weight and bodywater in patients on the highfat and the high-protein diets. The
high-carbohydrate diets are excluded because changes in
body-weight and body-water were negligible during this period.”

No figures for WATERRETENTION during the high-carb part of diet of series 2.

Why don’t you have anything to say about the Yang study with its much preciser measurments, which clearly shows that even if you gain weight when switching from a ketogenic diet to mixed diet you are still loosing fat tissue and the weight gain is due to waterretention?

You actually think this didn’t happen i the Kekwik study? It surely did and the data actually confirms it.

And you didn’t answer this question:

Were are the figures for fat loss during the fat-, protein-, and carb-based part of the diet 2 series?

You didn’t answer because you can’t. They didn’t measure fat loss in the Kekwik study unlike in the Yang-study where you can find figures for fat loss.

Subjects in the Yang study consumed from 600-800 kcal per day. At these low caloric intakes, one wouldn’t expect any difference in wt loss. I’ve made my case against the studies Colpo presented in his book once already; I’m not going to go back through and argue them all individually again. Colpo wrote his book; I critiqued it; he critiqued my critique. There’s an end on it. People who are interested – very few, I’m sure – can read both sides of the debate and come to their own conclusions. It’s obvious that you have come down on the Colpo side, and that’s fine with me. I don’t want to waste any more time diddling with it. If you want to continue the debate, be my guest, but you’re going to have to do it without me.

Page 158 of the Kekwick and Pawan study deals with all the questions you’ve been asking. If you are unable to figure this out from your reading of the paper, it’s not my obligation to educate you.

Apparently you are not reading what I am writing because I am NOT refering to; Yang – Metabolic effects of substituting carbohydrate for protein in a low-calorie diet: a prolonged study in obese patients

Sorry about that. I saw Yang and I thought of the Colpo-mentioned study. But it doesn’t really matter because I’ve already said I’m not going to start arguing and analyzing studies outside of the Colpo book.

To quote Aubrey de Gray on the subject, “any biologist in the audience will be perfectly familiar with the concept that we are actually unbelievably ignorant about how cells work, let alone how organisms work. So this is part of the problem: we just don’t know enough about metabolism.”

To all bloggers: more signal, less noise please. Resist resorting to the ad hominem stuff; in the end it does no good. I know how hard it is to resist attacking someone who has attacked or misrepresented you. I live in a glass house too.

Please (all) impress me and others with high quality discussion while treating others with dignity and respect (whether or not you think they deserve it. Show you are better by not taking the bait.

Steve L (maybe I will post this comment on other blogs to show I am trying to be even-handed here)